Mast cells (MCs) are innate immune cells originating from CD34+/C D117+ hematopoietic stem cells and regulate liver disease progression.[1] With a variety of surface receptors, MC activation is triggered by two main receptor-dependent pathways: IgE/high-affinity receptor for the Fc region of IgE (FcεRI) and IL-33/sup-pressor of tumorigenicity 2 (ST2).[2] Upon liver damage, MCs degranulate releasing mediators, including pre-formed bioactive metabolites (histamine, tryptase, and chymase), newly synthesized cytokines (TGF-β, TNF-α, and I L- 1β), and de novo lipid mediators (leukotriene B4, leukotriene D4, prostaglandin)[3] (Figure 1). TGF-β1, TNF-α, IL-6, IL-10, and synaptophysin 9 (SYP-9) are re-leased upon liver damage by paracrine interactions be-tween MCs and hepatocytes (through TGF-β,[4] TNF-α[5]), cholangiocytes (through IL-10, TGF-β[6]), HSCs (through SYP- 9, TGF-β1[7]), and Kupffer cells (through TNF-α, I L- 6[8 ]). This review encompasses the most recent stud-ies involving MCs, their mediators, and the impact on liver disease.
Mast cells in liver disease progression: an update on current studies and implications / Pham, Linh; Kennedy, Lindsey; Baiocchi, Leonardo; Meadows, Vik; Ekser, Burcin; Kundu, Debjyoti; Zhou, Tianhao; Sato, Keisaku; Glaser, Shannon; Ceci, Ludovica; Alpini, Gianfranco; Francis, Heather. - In: HEPATOLOGY. - ISSN 0270-9139. - 75:1(2022), pp. 213-218. [10.1002/hep.32121]
Mast cells in liver disease progression: an update on current studies and implications
Ceci, Ludovica;Alpini, Gianfranco;
2022
Abstract
Mast cells (MCs) are innate immune cells originating from CD34+/C D117+ hematopoietic stem cells and regulate liver disease progression.[1] With a variety of surface receptors, MC activation is triggered by two main receptor-dependent pathways: IgE/high-affinity receptor for the Fc region of IgE (FcεRI) and IL-33/sup-pressor of tumorigenicity 2 (ST2).[2] Upon liver damage, MCs degranulate releasing mediators, including pre-formed bioactive metabolites (histamine, tryptase, and chymase), newly synthesized cytokines (TGF-β, TNF-α, and I L- 1β), and de novo lipid mediators (leukotriene B4, leukotriene D4, prostaglandin)[3] (Figure 1). TGF-β1, TNF-α, IL-6, IL-10, and synaptophysin 9 (SYP-9) are re-leased upon liver damage by paracrine interactions be-tween MCs and hepatocytes (through TGF-β,[4] TNF-α[5]), cholangiocytes (through IL-10, TGF-β[6]), HSCs (through SYP- 9, TGF-β1[7]), and Kupffer cells (through TNF-α, I L- 6[8 ]). This review encompasses the most recent stud-ies involving MCs, their mediators, and the impact on liver disease.File | Dimensione | Formato | |
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